10 Spinal Ataxia II: EDM, EPM, and EHM

• Spinal Ataxia II encompasses:
  • Equine Degenerative Myeloencephalopathy (EDM)
  • Equine Protozoal Myelitis
  • Equine Herpesvirus Myeloencephalopathy

Equine Degenerative Myelopathy

• Affected horses struggle to assimilate vitamin E, leading to oxidative damage in the CNS.
• This results in spheroid formation in brainstem nuclei, neuraxonal dystrophy in lumbosacral and cervical intermediate gray columns.
• It also causes neuronal degeneration in ventral and dorsal spinocerebellar tracts, and ventromedial funiculi.
• Signalment includes horses aged 6 months to 2 years, with no gender predilection.
• It's familial in Standardbreds, Morgans, Thoroughbreds, Quarterhorses, and Zebras.
• Neurologic examination reveals symmetric gait deficits (prominent spasticity), with forelimb deficits equal to or worse than hind limbs.
• Neuroanatomic localization is diffuse spinal cord, with decreased cutaneous trunci reflex.
• Diagnosed by exclusion, it involves unremarkable CSF analysis, cervical radiographs, and myelographic examination.
• Serum vitamin E concentrations may be low, and necropsy examination requires submitting the medulla, pons, and thoracic spinal cord.
• Treatment involves Vitamin E supplementation (10,000 IU PO SID x 6 months, natural).
• Supplementation may prevent disease progression but is unlikely to reverse clinical signs.
• Neurologic dysfunction does not progress to recumbency, and signs plateau at 2 to 3 years of age, remaining stable throughout life.

Equine Protozoal Myelitis (EPM)

• Caused by the protozoal organism Sarcocystis neurona within the spinal cord and cerebrum/brainstem.
• Horses become infected via ingestion of opossum feces.
• Horses are dead-end hosts, and only asexual forms of the organism are seen in horses; horse-to-horse transmission does not occur.
• Sarcocystis neurona has a two-host lifecycle, with cats, skunks, raccoons, and armadillos serving as secondary hosts.
• The organism encysts in the secondary host muscle, completing its lifecycle when an opossum eats it.
• Clinical disease is reported in all breeds and ages, peaking from 15 months to 5 years, and rare in ponies or horses younger than 1 year.
• Its geographic distribution corresponds to opossum populations.
• Neurologic exams show the neuroanatomic localization depends on the organism's location in the central nervous system.
• Multifocal disease, asymmetric signs, and/or focal muscle mass loss should raise suspicion for EPM.
• Clinical signs may be insidious or acute, with progression being rapid, slow, or static.
• Cytologic evaluation during CSF analysis shows mild protein and total cell count elevation (mononuclear pleocytosis).
• Commercial testing is available.
• SAG-2, 4/3 ELISA uses the Serum to CSF ratio, and specificity approaches 100%.
• False negatives do occur. This is currently the most widely-used test.
• Multiplex SAG-1, 5, 6 is a horse-side test with high specificity, however the sensitivity is uncertain.
• Indirect Fluorescent Antibody Test (IFAT) is performed on serum or CSF samples (ideal for CSF samples with iatrogenic blood contamination.)
• Western blot identifies antibody against S. neurona.
• Serum testing indicates a 35-70% immunoblot analysis positive rate.
• A seropositive result does not confirm diagnosis, but a seronegative result rules out EPM.
• Detection of a positive CSF indicates intrathecal production of said anitbodies.
• False positives are common.
• Ponazuril (Marquis®) is the first FDA-approved drug for EPM treatment, and it attacks the chloroplast function of the protozoa.
• Diclazuril (Protazil®) is a top-dress pellet.
• Sulfadiazine, pyrimethamine (Rebalance®) must be administered on an empty stomach, and pyrimethamine is a dihydrofolate reductase inhibitor with high affinity for protozoal organisms.
  • Complications include colitis, anemia, neutropenia, and abortion; do not use in pregnant mares.
• Support includes sling support, good footing, and a safe environment.
• Most horses improve in 1 to 3 weeks after therapy initiation.
• Prognosis for complete recovery is less than 20%.
• The prognosis is poor if there's recumbency and more favorable for brainstem dysfunction than spinal cord signs.
• To prevent EPM the hay and pasture should not be contaminated with possum feces.
• Contaminated water sources and grain may also be a source for infection. Secure grain and hay, relocate possums, and remove cat, skunk, etc.

Equine Herpes Myeloencephalitis (EHV-1)

• Signalment includes a history of fever 5 to 7 days before neurologic signs onset, with no gender, breed, geographic, or seasonal predilection.
• Aged horses are predisposed to experimental infections.
• The number of outbreaks and morbidity/mortality is on the rise. The USDA designated neuropathic EHV as a "potentially emerging" disease in 2007. and was the subject of the 2009 ACVIM consensus statement.
• Morbidity for developing during an outbreak is 26%.
• Mortaility in horses with neurologic signs is 29%.
• Symptoms include ascending myelitis, symmetric weakness and ataxia, worse rear limb deficits, poor tail tone, urine dribbling, and prolapsed penis.
• CSF analysis reveals xanthochromia, moderate to marked protein elevation, and normal CSF cell count consisting of small lymphocytes.
• Use Nested PCR (24 hr) and virus isolation to identify the neuropathic strain
• Treatments include isolation from other horses for 21 days of resolution.
• Antiviral therapy of valacyclovir or IV acyclovir are also an option.
• Supportive care of urinary catheterization and sling are also an option.
• Vaccination can reduce the magnitude and duration of viral shedding, which may reduce the spread of infection through premises.